Alzheimer's disease (AD) is a kind of dementia, of which the major symptoms include a cognitive decline and a personality change. Dementia is a common disease by which approximately 25% of Japanese elderly people of age 85 or older are affected, and AD accounts for about 50% of all kinds of dementia. As of 2011, Japan has approximately 1.6-1.8 million AD patients, the number of which should go on rising as the elderly people account for an increasing percentage of the world population in the future. This is a particularly serious problem for Japan, in which the number of children per household has been falling while the number of elderly people has been rising recently.
An acetylcholinesterase inhibitor, which is believed to be most effective in preventing and treating AD, is in fact only partially effective for patients with a mild or moderate degree of disease, and its effectiveness for patients with an advanced degree of disease is denied by a lot of people.
Although AD is actually characterized by senile plaque of β amyloid and by Neurofibrillary Tangles (NFT) formed by abnormal tau protein polymerization, recent neuropathological comments about AD patients indicate that the current mainstream AD research is based on an amyloid β hypothesis that an abnormal amyloid β peptide triggers the AD symptom.
However, it has recently been found that in the familial frontotemporal dementia (FTDP), the dementia symptom expresses itself due the formation of NFTs promoted by the mutation of a tau gene, and abnormality is caused in nerve cells just by aggregation and accumulation of the tau protein in the brain. Thus, people have recently been paying a lot of attention to the correlation between the tau aggregation and the onset of AD.
The tau protein is a kind of protein which is present in profusion in central nerve cells and which is indispensable for the neuroaxis that forms a neural network in the brain to function properly. However, once the tau protein formed an insoluble aggregate in cells, the axonal transport would no longer work fine to cause the death of nerve cells.
Patent Document 1 discloses a drug which includes, as its main ingredient, a naphtho quinone compound that inhibits the tau aggregation in order to alleviate the symptom of AD. With this drug, the tau aggregation in cells is reduced to a certain extent, and therefore, the formation of NFTs is suppressed to the point that the symptom of AD is alleviated.